Obesity in the U.S. is an epidemic with 65% of adults and 25% of children being overweight or obese. Obesity predisposes to Type 2 diabetes in adults and children. This project began with the identification of a new form of obesity in a child caused by disrupting a gene called SIM1. A mouse was created that had a similar genetic defect and this mouse was also found to be obese due to overeating. Our project focuses on studying this mouse line. The importance of this gene is highlighted by the fact that it functions in the part of the brain that manages how much we eat. In this project we are defining how this gene works with other genes known to be important in regulating food intake. We will treat our mouse with drugs that we believe work beyond the block caused by this gene to attempt to rescue it from obesity. These results could lead to new targets for drugs to prevent or treat obesity. This could greatly impact our ability to prevent type 2 diabetes and coronary artery disease, major public health threats in the United States and other nations.
SIGNIFICANT PUBLICATIONS
Kublaoui B, Lee J, Pilch PF, "Dynamics of signaling during insulin- stimulated endocytosis of its receptor in adipocytes" J Biol Chem, 270:59-65, 1995
Liu H, Kublaoui B, Pilch PF, Lee J, "Insulin activation of mitogen activated protein (MAP) kinase and Akt is phosphatidylinositol 3-kinase dependent in rat adipocytes" Biochem Biophys Res Commun, 274(3):845-51, 2000
Holder JL Jr, Zhang L, Kublaoui BM, DiLeone RJ, Oz OK, Bair CH, Lee YH, Zinn AR, "Sim1 gene dosage modulates the homeostatic feeding response to increased dietary fat in mice" Am J Physiol Endocrinol Metab, 287(1):E105-13, February 2004
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